Lesson of the Week Phosphate enemas in childhood: cause for concern M McCabe, J R Sibert, P A Routledge
Phosphate enemas should be used with caution in children aged over 3 years and avoided in younger children
Department of Child Health and Welsh National Poisons Unit, University of Wales College of Medicine, Llandough Hospital, Penarth, South Glamorgan CF6 lXX M McCabe, MRCPI, senior registrar in accident and emergency medicine J R Sibert, MD, consultant paediatrician (community
child health) P A Routledge, MD, professor of clinical pharmacology Correspondence to: Dr Sibert. BMJ 1991;302:1074
Phosphate enemas are generally thought to be nontoxic to children and not absorbed in appreciable quantities. A recent report on the toxicity of magnesium sulphate enemas implied that phosphate enemas might be an alternative.' The British National Formulary states only that "the dose should be reduced in children."' However, there have been several reports from North America of the absorption and toxicity of phosphate enemas,3s one of which was fatal. We report a case of severe toxicity due to such an enema.
1 07 mmol/l, and phosphate 4-5 mmol/l, suggesting absorption of the contents of the enema. Calcium gluconate (10 ml of a 10% solution) was given intravenously during an hour. An infusion of half strength physiological saline and 2 5% dextrose was continued after the plasma. The large faecal mass was digitally evacuated, and the patient's condition improved. Her serum electrolyte concentrations showed a gradual return to normal, and she was discharged seven days subsequently, having achieved frequent passage of normal stools with increased doses of laxatives.
Case report A girl aged 2 years 8 months with the cri du chat syndrome due to an unbalanced translocation involving chromosome 5 and developmental delay had a severe problem with constipation. She had pulmonary atresia and a ventricular septal defect, and she was being treated with diuretics for cardiac failure. Constipation had become a problem from about the age of 2 years. The use of several laxatives and sodium citrate (Micralax) enemas at home had not been generally successful, and a series of day case admissions was planned for giving phosphate enemas. On the first admission 90 ml of a phosphate enema (Fletcher's phosphate enema, Pharmax UK, containing sodium acid phosphate BP 12 8 g and sodium phosphate 10 24 g made up to 128 ml aqueous solution) was given by a sister trained as a children's nurse. The girl was observed for several hours and subsequently allowed home. There was a small return of fluid faeces after the enema. She was readmitted some hours later drowsy, grey, and ill, with a pulse rate of 120 beats/min, a temperature of 37 2 °C, and blood pressure of 70/50 mm Hg. On examination of her abdomen she had abdominal fullness and marked tenderness in the left iliac fossa. Bowel sounds were decreased. x Ray films showed dilated loops of bowel with a large faecal mass in the rectum and no air under the diaphragm. The differential diagnosis was of absorption of the contents of the enema or possible. perforation of the rectum. An intravenous infusion with physiological saline progressing to plasma was started, with intravenous cefotaxime 500 mg twice daily and metronidazole 80 mg thrice daily. Laboratory investigations disclosed serum concentrations of sodium of 150 mmol/l, potassium 2-8 mmol/l, bicarbonate 18 mmol/l, calcium
Discussion This case shows that a life threatening condition may occur as a result of a simple, commonly used treatment. There had been no such previous reports in Britain, although several cases have been reported in North America,46 including the death of an 8 month old infant in Honolulu. Some experimental work was done on anaesthetised pigs to find a mechanism for the incident, in which seven pigs were given graded doses of a phosphate enema (Fleet, United States) through the rectum with a Foley catheter. Above a certain dose (30 ml/kg) all the pigs died, owing to sodium phosphate being absorbed systemically, leading to profound metabolic changes. The advice note in the British National Formulary only cautions about reducing the dose in children but does not give any other specific information. The data sheet by Pharmax, on the other hand, does not recommend the use of phosphate enemas in children aged under 3 years, and advises their use in those aged over 3 according to body weight. We recommend that phosphate enemas should not be used in children aged under 3 years, and that they should be used only with caution at reduced doses in older children. I Ashton MR, Sutton 1), Nielsen M. Severe magnesium toxicity after magnesium sulphate enema in a chronically constipated child. BMJ 1990;300:541. 2 British National Formularv. London: British Medical Association and Royal Pharmaceutical Society of Great Britain, March 1990:70. 3 Sotos JF, Cutler EA, Finkel MA, Doody D. Hypocalcemic coma following two pediatric phosphate enemas. Pediatrics 1977;60:305-7. 4 Davis RF, Eichner JM, Bleyer A, Okamoto G. Hvpocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema.
JIPediatr 1977;90:484-5. 5 Forman J, Baluarte HJ, Gruskin AB. Hypokalemia after hypertonic phosphate enemas. 7 Pediatr 1979;94:149-51. 6 M\artin RR, Lisehora GR, Braxton M Jr, Barcia PJ. Fatal poisoning from sodium phosphate enema. JAMA 1987;257:2 190-2. 7 Pharmax UK. Data sheet: Fletchers' phosphate enema. Bexley, Kent: Pharmax, 1990. (Accepted 21lanuarv 1991)
ANY QUESTIONS Should an otherwise fit patient suffering a grand mal seizure be given oxygen? Most major convulsive seizures are of short duration, and the anoxia that results from the interruption of respiration, even if the patient becomes cyanosed, does not usually have any long term consequences. The cyanosis is due to the cessation of ventilation, so that oxygen supplied by a facemask would have little effect, and adequate oxygenation occurs quickly
1074
once normal breathing resumes. It is therefore unnecessary to give patients an oxygen supply at home. In prolonged seizures, as may occur with febrile convulsions in infancy, in which the anoxia is thought to lead to mesial temporal sclerosis, and in status epilepticus in adults, oxygen should be administered by high flow facemask as part of the resuscitation. But the priority should be to stop the seizure as soon as possible, making oxygen unnecessary. -M D O'BRIEN, physician for nervous diseases, London
BMJ VOLUME 302
4 MAY 1991
Phosphate enemas should be used with caution in children aged over 3 years and avoided in younger children
Department of Child Health and Welsh National Poisons Unit, University of Wales College of Medicine, Llandough Hospital, Penarth, South Glamorgan CF6 lXX M McCabe, MRCPI, senior registrar in accident and emergency medicine J R Sibert, MD, consultant paediatrician (community
child health) P A Routledge, MD, professor of clinical pharmacology Correspondence to: Dr Sibert. BMJ 1991;302:1074
Phosphate enemas are generally thought to be nontoxic to children and not absorbed in appreciable quantities. A recent report on the toxicity of magnesium sulphate enemas implied that phosphate enemas might be an alternative.' The British National Formulary states only that "the dose should be reduced in children."' However, there have been several reports from North America of the absorption and toxicity of phosphate enemas,3s one of which was fatal. We report a case of severe toxicity due to such an enema.
1 07 mmol/l, and phosphate 4-5 mmol/l, suggesting absorption of the contents of the enema. Calcium gluconate (10 ml of a 10% solution) was given intravenously during an hour. An infusion of half strength physiological saline and 2 5% dextrose was continued after the plasma. The large faecal mass was digitally evacuated, and the patient's condition improved. Her serum electrolyte concentrations showed a gradual return to normal, and she was discharged seven days subsequently, having achieved frequent passage of normal stools with increased doses of laxatives.
Case report A girl aged 2 years 8 months with the cri du chat syndrome due to an unbalanced translocation involving chromosome 5 and developmental delay had a severe problem with constipation. She had pulmonary atresia and a ventricular septal defect, and she was being treated with diuretics for cardiac failure. Constipation had become a problem from about the age of 2 years. The use of several laxatives and sodium citrate (Micralax) enemas at home had not been generally successful, and a series of day case admissions was planned for giving phosphate enemas. On the first admission 90 ml of a phosphate enema (Fletcher's phosphate enema, Pharmax UK, containing sodium acid phosphate BP 12 8 g and sodium phosphate 10 24 g made up to 128 ml aqueous solution) was given by a sister trained as a children's nurse. The girl was observed for several hours and subsequently allowed home. There was a small return of fluid faeces after the enema. She was readmitted some hours later drowsy, grey, and ill, with a pulse rate of 120 beats/min, a temperature of 37 2 °C, and blood pressure of 70/50 mm Hg. On examination of her abdomen she had abdominal fullness and marked tenderness in the left iliac fossa. Bowel sounds were decreased. x Ray films showed dilated loops of bowel with a large faecal mass in the rectum and no air under the diaphragm. The differential diagnosis was of absorption of the contents of the enema or possible. perforation of the rectum. An intravenous infusion with physiological saline progressing to plasma was started, with intravenous cefotaxime 500 mg twice daily and metronidazole 80 mg thrice daily. Laboratory investigations disclosed serum concentrations of sodium of 150 mmol/l, potassium 2-8 mmol/l, bicarbonate 18 mmol/l, calcium
Discussion This case shows that a life threatening condition may occur as a result of a simple, commonly used treatment. There had been no such previous reports in Britain, although several cases have been reported in North America,46 including the death of an 8 month old infant in Honolulu. Some experimental work was done on anaesthetised pigs to find a mechanism for the incident, in which seven pigs were given graded doses of a phosphate enema (Fleet, United States) through the rectum with a Foley catheter. Above a certain dose (30 ml/kg) all the pigs died, owing to sodium phosphate being absorbed systemically, leading to profound metabolic changes. The advice note in the British National Formulary only cautions about reducing the dose in children but does not give any other specific information. The data sheet by Pharmax, on the other hand, does not recommend the use of phosphate enemas in children aged under 3 years, and advises their use in those aged over 3 according to body weight. We recommend that phosphate enemas should not be used in children aged under 3 years, and that they should be used only with caution at reduced doses in older children. I Ashton MR, Sutton 1), Nielsen M. Severe magnesium toxicity after magnesium sulphate enema in a chronically constipated child. BMJ 1990;300:541. 2 British National Formularv. London: British Medical Association and Royal Pharmaceutical Society of Great Britain, March 1990:70. 3 Sotos JF, Cutler EA, Finkel MA, Doody D. Hypocalcemic coma following two pediatric phosphate enemas. Pediatrics 1977;60:305-7. 4 Davis RF, Eichner JM, Bleyer A, Okamoto G. Hvpocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema.
JIPediatr 1977;90:484-5. 5 Forman J, Baluarte HJ, Gruskin AB. Hypokalemia after hypertonic phosphate enemas. 7 Pediatr 1979;94:149-51. 6 M\artin RR, Lisehora GR, Braxton M Jr, Barcia PJ. Fatal poisoning from sodium phosphate enema. JAMA 1987;257:2 190-2. 7 Pharmax UK. Data sheet: Fletchers' phosphate enema. Bexley, Kent: Pharmax, 1990. (Accepted 21lanuarv 1991)
ANY QUESTIONS Should an otherwise fit patient suffering a grand mal seizure be given oxygen? Most major convulsive seizures are of short duration, and the anoxia that results from the interruption of respiration, even if the patient becomes cyanosed, does not usually have any long term consequences. The cyanosis is due to the cessation of ventilation, so that oxygen supplied by a facemask would have little effect, and adequate oxygenation occurs quickly
1074
once normal breathing resumes. It is therefore unnecessary to give patients an oxygen supply at home. In prolonged seizures, as may occur with febrile convulsions in infancy, in which the anoxia is thought to lead to mesial temporal sclerosis, and in status epilepticus in adults, oxygen should be administered by high flow facemask as part of the resuscitation. But the priority should be to stop the seizure as soon as possible, making oxygen unnecessary. -M D O'BRIEN, physician for nervous diseases, London
BMJ VOLUME 302
4 MAY 1991
